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Sci. Signal., 25 January 2011
Vol. 4, Issue 157, p. ra5
[DOI: 10.1126/scisignal.2001279]

RESEARCH ARTICLES

Editor's Summary

Acting Locally as Well as Globally
Arginine vasopressin (AVP), which acts as an antidiuretic hormone to decrease plasma osmolarity, is synthesized by osmosensory hypothalamic neurons and released from their terminals in the posterior pituitary into the systemic circulation. Consistent with this homeostatic role, increased plasma osmolarity increases nerve terminal release of AVP, whereas decreased plasma osmolarity decreases it. Here, Sato et al. show that, in contrast to its effect on systemic secretion of AVP, hypo-osmotic stimulation of isolated AVP neurons increased somatodendritic AVP release. AVP acted through the V2 receptor to activate volume-sensitive anion currents and initiate a slow decrease in AVP neuron volume, counteracting the swelling induced by exposure to hypo-osmotic solution. The authors thus conclude that somatodendritic release of AVP acts as an autocrine signal to help AVP neurons maintain an appropriate volume while undergoing hypotonic stress.

Citation: K. Sato, T. Numata, T. Saito, Y. Ueta, Y. Okada, V2 Receptor–Mediated Autocrine Role of Somatodendritic Release of AVP in Rat Vasopressin Neurons Under Hypo-Osmotic Conditions. Sci. Signal. 4, ra5 (2011).

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